The basic objectives remain unchanged: to determine the hormonal (and other) factors regulating the growth and regression of follicles and corpora lutea in the mammalian ovary. Six broad projects are contemplated: 1. We have found specific FSH binding sites in hamster oocytes. Are they present in other species? What are the functions of the receptors? What hormones regulate the numbers of receptors? Are there quantitative differences in numbers of FSH binding sites during folliculogenesis? 2. By combining 3 enzymes we can disperse within 20 minutes all follicles-from primordial to Graafian-in hamster ovaries. This provides a technique for analysis of follicular kinetics in detail: steroidogenesis, DNA, receptors, response to steroids and gonadotropins. 3. Cycloheximide injected into proestrous hamsters prevents ovulation the next day and delays by several hours the estrogen-progesterone shift in follicular secretion pattern. What are the mechanisms involved? 4. A single injection of anti-LH serum induces superovulation of 30 ova in cyclic hamsters and pregnant mice but is ineffective in cyclic or pregnant rats. Why? What are the mechanisms of action of anti-LH? 5. The hamster ovary-unlike the rat-does not respond to massive injections of estrogen by increased numbers of preantral follicles yet the uterus responds by increased weight. What is the basis for this species difference and what about other species. Is the difference attributable to lack of ovarian estrogen receptors? 6. Work from this lab established the concept of a luteotropic (Lth) complex which regulates the corpora lutea of many species of mammals. In the hamster, FSH serves as a constituent of Lth complex. Advances in purification of peptide hormones and other procedures, make it possible to re-explore this problem and to determine whether FSH (without LH contamination) can function as a luteotropic hormone. The research is related to both fertility control and infertility. Work will proceed on a broad front.